Synthetic tuftsin-derived heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) for in vitro anxiolytic-pathway, BDNF, and monoaminergic research.
Every batch of Selank is sent to an accredited independent laboratory before it ships. Here is exactly what we screen for - and the certificate that proves it.
Tuftsin-derived heptapeptide studied across anxiolytic, neurotrophic, and immunomodulatory in vitro models
Selank dose-dependently inhibits plasma enkephalin-degrading enzymes (IC50 ~15 µM), prolonging endogenous enkephalin signaling. Preclinical models also report modulation of GABA-A receptor expression in cortical and hippocampal tissue, producing anxiolytic-like activity without sedation or motor impairment.
Intranasal Selank in rat models upregulates BDNF mRNA in the hippocampus within hours of administration. Selank also accelerates 5-HT metabolism in the hypothalamus and brain stem, raising 5-HIAA/5-HT ratios — including in PCPA-pretreated animals where intrinsic serotonin synthesis is blocked.
The N-terminal TKPR (tuftsin) fragment retains immunomodulatory activity. Selank shifts cytokine balance in preclinical and clinical research models, with documented effects on IL-6 and interferon-gamma profiles in anxiety-asthenic disorder cohorts.
Key findings from peer-reviewed preclinical and clinical publications
Primary areas of Selank preclinical investigation
Elevated plus maze and open field paradigms in rodents document anxiolytic-like activity comparable to benzodiazepines without sedation, motor impairment, or dependence liability — a research model for non-GABA-A direct anxiolytic mechanisms.
Zolotarev et al. 2001 ↗Intranasal Selank rapidly upregulates BDNF mRNA in the rat hippocampus, with transient protein dip followed by sustained elevation. Used as a research model for peptide-mediated neurotrophic factor regulation.
Inozemtsev et al. 2010 ↗The N-terminal TKPR (tuftsin) fragment is a classical immunomodulator. Selank provides a metabolically stable scaffold for investigating tuftsin-receptor pharmacology and cytokine network modulation (IL-6, IFN-γ).
Uchakina et al. 2008 ↗Selank elevates 5-HIAA/5-HT ratios in rat hypothalamus and striatum, accelerating serotonin turnover. Effects persist in PCPA-pretreated animals, supporting research into post-synaptic monoamine signaling.
Semenova et al. 2009 ↗Technical specifications and analytical profile
Common questions about Selank research parameters
Peer-reviewed PubMed-indexed publications

$40 value — free with any order over $99
You're in! Use this code at checkout:
Add a GHK-Cu vial and apply the code on orders over $99.
Limit 1 per customer
For laboratory research purposes only. Not for human consumption, medical, veterinary, household, or any other use.